2. Overview
• Severe preeclampsia – pathophysiology, Dx, maternal/fetal issues,
Treatment
• Case - Ante partum flash Pulmonary edema
• Discussion

3. PREECLAMPSIA
A syndrome characterized by the new onset of hypertension and
proteinuria after 20 weeks gestation. Additional signs and
symptoms that can occur include edema, visual disturbances,
headache, epigastric pain, thrombocytopenia, and abnormal liver
function. These clinical manifestations are the results of
mild to severe microangiopathy of target organs such as brain,
liver, kidney, and placenta.

4. PATHOPHYSIOLOGY OF PREECLAMPSIA
A state of endothelial dysfunction secondary to excessive amounts
of circulating factors released from the diseased placenta. These
factors effect the establishment of a suitable vascular network of the
placenta needed to supply oxygen and nutrients to the fetus.
• Molecular/Cellular level
– Abnormal expression of VEGF and sFlt-1 (Vascular
endothelial growth factor –proangiogenic and soluble fms-like
tyrosine kinase 1- anti-angiogenic factors respectively) appear
to play a central role.
– Increased expression of cytokines, angiotensin,
catecholamines, and pro-coagulant factors.
• Anatomic level
– Increased vascular tone
– Increased vascular permeability
– Coagulopathy
– Ischemia of target organs (brain, liver, kidney, placenta)

5. Multisystemic Disease
• CNS – Cortical blindness, cerebral edema, cerebral hemorrhage, and seizures
• Cardiovascular – Hypovolemia, increased SVR, LVH, increase sensitivity to catecholamines,
sympathomimetics, and oxytocin
• Respiratory – pulmonary edema, V/Q mistmatch, airway edema
• Renal – Decreased renal blood flow, increased GFR, proteinuria, increased BUN and creatinine
• Hepatic – subscabular hemorrhage, abnormal LFTs, decreased plasma cholinesterase levels
• Hematologic – Prolonged bleeding time, platelet dysfunction, thrombocytopenia, DIC
• Placenta – Uteroplacental insufficiency, placental abruption, chronic fetal hypoxia, IUGR,
premature labor, premature birth.

6. Diagnosis of Severe Preeclampsia
If one or more of the following criteria are present:
• Systolic blood pressure > 160 mmHg
• Diastolic blood pressure greater than 110 mmHg
• Proteinuria greater than 5 g/24 hrs
• Evidence of end organ damage
–Oliguria (<500ml/24hr)
–Cerebral or visual disturbances
–Pulmonary edema or cyanosis
–Epigastric pain or right upper-quadrant pain
–Impaired liver function
–Fetal growth restriction
–Thrombocytopenia
*ACOG Compendium of Selected Publications

7. Goals
• Control CNS irritability
– Magnesium sulfate – anti-convulsant; reduces irritability of the
neuromuscular jxn.
• Restore intravasuclar fluid volume
– Strictly monitor urine output
– CVP monitor with goal 4-6 cm H20
• Normalize blood pressure
– Magnesium sulfate – direct vasodilating action on smooth
muscles of arterioles and uterus.
– Labetolol, Hydralazine, nifedipine, SNP (in extreme
circumstances due to fetus susceptability to cyanide toxicity)
• Correct coagulation abnormalities
– Platelets, FFP, Cryoprecipitate

8. Effects of Increasing Plasma Magnesium Levels
• MgSO4 in excess of therapeutic range
– Skeletal muscle weakness
– Respiratory depression
– Cardiac arrest (Ca++ can counter-act this)
– MgSO4 potentiates NMB and sedative effects of opiods
Observed Condition mEq/L
Normal Plasma level 1.5-2.0
Therapeutic Range 4.0-8.0
ECG Changes (Prolonged P-Q, widened QRS) 5.0-10
Loss of deep tendon reflexes 10
SA and AV node block 15
Respiratory Paralysis 15
Cardiac Arrest 25

9. Functional effects
Anatomical Effects Functional Effects
Airway edema
friability
Widened AP and
Transverse diameter
Elevated
Diaphragm
Widened Subcostal
angle
Enlarging uterus
Increased respiratory drive
Minimal change in TLC
Increased Minute ventilation
Reduced FRC
Normal diaphramatic Fxn
Increased O2 consumption
and CO2 production
www.medtau.org
Increased cardiac output

10. Management
Definitive treatment for Preeclampsia is delivery of the fetus and placenta.
• Vaginal Delivery – Lumbar epidural
– No fetal distress
– Before catheter placement, r/o coagulopathy and insure adequate
volume replacement.
• Cesarean Delivery – Regional or GA
– Maternal/and or fetal status dictates the urgency for delivery
– Use epidural if in place. Maintain volume status. Typically, drops in
BP improve placental blood flow.
– Spinal anesthesia, in the past, has been controversial due to possibility
of severe hypotension. However, it has been shown to be a safe
technique for cesarean delivery in severe preeclampsia.
– General anesthesia is an acceptable way to manage preeclamptic pts,
however, there are associated risks.
• Apiration
• Airway compromise
• Cerebral hemmorrhage
• Pulmnary Edema

11. Case Report
Personal Hx
• Mrs N. Safi
• 38 yrs .
• Married for 16 yrs.
• G6P5L4
• Pregnant at full term.
• Was brought to our Emergancy Department on 25.9.2011 at
1:45 am .

12. Chief complain:
• Sudden coughing, dyspnea and choking.
Hx of present illness :
• Pt complained of sudden onset coughing,
dyspnea and choking
• She had suffered from persisted headache for four
days.
Obstetric Hx
• She had 4 living baby product of 4 uncomplicated
normal vaginal deliveries.
• No previous miscarriage .
• Her previous pregnancies was smooth except for
mild PIH in the first pregnancy.
• She was unbooked (Only one visit to P.H.C at 4
month of gestation).

13. Gynecologic Hx: Normal menarche & menses.
Past Hx : Uneventful
Drug Hx: None
Family Hx : Mother and father are hypertensive

14. on Admission
PHYSICAL EXAMINATION
Unconscious , extreme dyspnea, marked cyanosis
and blood-stained frothy mucus streamed from
her nose and mouth.
Vital Signs:
• T= 37.1oC BP= 270/150 mmHg
• RR= 25 bpm HR=120 bpm R bil
• SpO2 = 74%
• There is moderate bilateral biting LL edema extending up to
Knees.

15. on Admission
• Chest: Large bubbling rales were heard on both sides
• Abdomen: extended with gravid uterus .FL± 34 Wk
• Cardiac: RRR, no murmur appreciated, no JVD.
• Fetal heart heart by Doppler
• Vaginal examination: Closed unfavorable cervix

16. In summary,,,
• Mrs N. Safi is 38 yrs , P4+oL4,Preg. At FT admitted as case
of severe hypertension associated with extreme dyspnea,
marked cyanosis and blood-stained frothy mucus streamed
from her nose and mouth.

18. The Impression
• Pulmonary edema complicating severe
preeclampsia.
• Pulmonary edema likely secondary to
malignant hypertension

19. PROGRESS IN HOSPITAL
• 2 IV Line.
• Oxygen support
• Control of BP
• Urgent Intubation.
• Lasix administered to resolve pulmonary edema.
• Urgent CS.

20. Control of BP
• Hydralazine: 10 mg IV bolus (repeated twice)
followed with IV infusion.
• Lasix: 20mg IV

21. Urgent CS At 02:00amAt 02:00am
• Started at 2:30 am … finish 3:05pm.
• Strait forward surgery
• Female baby, 3 Kg with apgar score: 8-10
• Ascetic
• 2 cytotec tab rectally.
• 20 mg Lasix.
• Heparin 5000u IV.
BP Pulse SPO2
Preoperative 190/125 141 94%
At the end of Op. 126/86 115 100%

22. Postoperative Progress
• Pt remained intubated. Transferred to the ICU for
care/post-op mgmt.
• Antihypertensive treatment (hyrdalazine infusion)
• MgSO4
• IV antibiotic.
• Heparin 5000u 1*2.
• Sedation.
• Cardiology Consultation.

23. INVESTIGATIONS
• BG:BG: A+veA+ve
• CBC :CBC :
• Chemistry :Chemistry :
WBC HB PLT
14.3 12.5 154000
AST ALT RBS urea Uric
dcid
creat
48 41 130 14 5.9 0.7

24. INVESTIGATIONS
• chemistry:chemistry:
• Urine analysisUrine analysis
• TSH: 2.6 T4: 8.4
WBC RBC Protien
13-15 0-2 +++
Na K Ca cl
140 4.3 8.2 109

25. Post op events (Day 1)
• Pt was extubated POD#1.
• BP 140-180/90-95
• Urine output: normal
• MgSO4 continue for 24hr.
• Atenolol 100mg 1*1
• Nifedipine 20mg 1*2

26. Cardiology Consultation
• ECG:Sinus tachycardia
• Echocardiogram: Good left ventricle
contraction, normal dimension and function.
Valves were normal .LVEF -60% and no
pericardial effusion

27. Post op events
• Pt transferred to postnatal ward in POD2.
• Remained stable
• Discharged on postoperative D5 in good general
condition on Atenolol 100mg 1*1 +Nifedipine
20mg 1*2 and advised to bee followed in medical
out patient clinic for treatment of hypertension.

28. Acute Pulmonary Edema
• Pulmonary edema is defined as the accumulation
of fluid in the pulmonary interstitial spaces and
alveoli,
• Which prevents the adequate diffusion of both
oxygen and carbon dioxide.

29. The pathogenesis of pulmonary edema
complicating pre-eclampsia-
• Generalised arterial vasospasm resulting in an increased
systemic vascular resistance (increased after load).
• Reduced plasma volume (decreased pre-load), and increased
left ventricular stroke work index (hyper dynamic heart).
• Impaired renal function.
• Serum albumin is reduced and capillary permeability is
increased due to endothelial damage.
All these changes predispose to an increased risk of pulmonary
edema.

30. Acute Pulmonary Edema in Pregnancy
• Cohort study(Anthony C. Sciscione et al) – 62,917 consecutive
pregnancies from 1989-1999, to describe the incidence,
predisposing factors contributing to pulmonary edema in the
pregnant patient.
– Fifty-one women (0.08%) were diagnosed with acute
pulmonary edema during ante partum - post partum period.
– 24 patients (47%) antepartum
– 7 patients (14%) intrapartum
– 20 patients (39%) post partum
• Most common causes:
– Tocolytics (25.5%) most commonly MgSO4 and SC terbutaline
– Cardiac disease (25.5%)
– Fluid overload (21.5%)
– Preeclampsia (18%)

31. Acute Pulmonary Edema in Pregnancy
In a study of 37 cases of pre-eclampsia, Sibai et al reported an
• incidence of pulmonary edema in 2.9% patients
• 30% of these cases developed pulmonary edema antenatally,
whilst 70% developed it after delivery, within an average
time of 71 hours.
• The mechanisms responsible for this increased incidence in
the post-partum period are recently reviewed by Benedetti et
all and Hankins et al, and are related to delayed post-partum
mobilisation of extracellular fluids.
• The incidence of pulmonary edema is influenced by pre-
existing chronic hypertension, maternal age and parity
→ 7.1% in patients with chronic hypertension as compared to l .
7% in those with pure pre-eclampsia.
→patients with maternal age of 26. 8 years have higher
incidence than those with mean age of 20.7 years.

32. Acute Pulmonary Edema in Pregnancy
• A report by Donnelly and Lock, on 533 patients who died of
toxaemia showed that pulmonary edema was a cause of
death in 25% cases.
• However, though it is a major cause of obstetric mortality, its
incidence is infrequent in well managed cases of pre-
eclampsia

33. Risk Factors
• Preeclampsia/eclampsia
• Tocolytic therapy
• Sever infection
• Cardiac disease
• Iatrogenic fluid overload
• Multiple gestation

34. EBM Discussion on Anesthetic Technique for
Cesarean Section for Severe Preeclampsia
• Randomized comparison of general and regional anesthesia
for cesarean delivery in pregnancies complicated by severe
preeclampsia (1995)
– Eighty women who required C/S
– Randomized - epidural/CSE/General
– Intra-operative BP compared in all groups
– No statistical or clinical difference in maternal or fetal
outcome
– Aside from logistical implications, general as well as
regional were shown to be equally acceptable if steps are
taken to ensure careful approach to either method.

35. EBM Discussion on Anesthetic Technique for
Cesarean Section for Severe Preeclampsia
• Prospective cohort study; Patients with severe preeclampsia
experience less hypotension during spinal anesthesia for
elective cesarean delivery than healthy parturients (2003).
• Compared incidence and severity of spinal anesthesia
associated hypotension in severe preeclamptic (n=30) vs.
healthy parturient (n=30).
– Under spinal, mean BP decreased by 32-39% in severe
preeclamptics and 33-60% in the healthy parturient.
– Healthy patients were given more ephedrine than the
preeclamptics for hypotension. Possible explained by
increased sensitivity of pressor drugs in the
preeclamptic.
• Findings suggest that the incidenc of severity of spinal
hypotension in preeclamptic patients with severe
hypertension may be less than previously believed.

36. Discussion
• Most likely cause of pulmonary edema is multifactorial. No
specific etiology was assigned.
• Unsuspected cardiac findings were common, and there was a
high incidence of valvular disease.
• Most pts had severe systolic dysfunction and LVH and not
cardiac disease.
• Underlying cardiac disease is most likely under-diagnosed
and under-reported due to under-use of echocardiography.

37. Discussion
• Although an uncommon event in pregnancy,
• it is associated with an increased risk of maternal and fetal
morbidity and mortality.
• Several risk factors have been identified: preeclampsia or
eclampsia, use of tocolytic therapy, severe infection, cardiac
disease, iatrogenic fluid overload,and multiple gestation.
• The physiologic changes associated with pregnancy may
predispose the pregnant patient to pulmonary edema.
• Despite the multiple causes of pulmonary edema, there is no
clear consensus on the role that each of these risk factors
plays in the pregnant population.

38. Conclusion
• Early diagnosis and management of
pulmonary edema in pregnancy is critically
important to improve maternal and neonatal
out come.
• Termination of pregnancy for patients with
pulmonary edema complicating severe pre-
eclampsia is mandatory.
• Echocardiography should be performed
early to evaluate the patient for possible
underlying cardiac disease.

39. Thank You